GH activation is mediated by many signalling pathways including the JAK2-STAT pathway.

• So body fat content is reduced, lean body mass increases along with metabolic rate.

Other metabolic actions:
Positive nitrogen and phosphorous balance.
Metabolic rate is increased, serum cholesterol is reduced.
Na and K+ retention. (not adrenal gland mediated)
Rise in plasma phosphoros, positive nitrogen balance (but lower serum amino acid levels)
Decrease in blood urea nitrogen.
Apparently, there's an increase in urine ammonia excretions despite a positive nitrogen balance. Source and Source

Vitamin D = cholecalciferol.
7-dehydrocholesterol -> + sunlight -> previtamin D3 -> Vitamin D3 --> action liver -> 25-hyroxy cholecalciferol (calcidiol) -> action of kidney -> 1,25 dihydroxy cholecalciferol. (calcitriol)

Activated vitamin D (1,25 dihydroxyvitamin D) regulates gene transcription by binding to intracellular receptors.
Mechanism: dihydroxycholecalciferol binds to it's receptor and acts as a transcription regulator which increases calbindin D proteins.
This proteins increases intestinal calcium absorption.
Induction of another protein in the renal tubules increases renal calcium absorption.

• Stimulation of osteoblast function and matrix calcification.
• permissively allowing PTH-induced osteoclast activation and bone resorption. (indirect osteoclast activation)
  The renal 1-alpha-hydroxylase enzyme which activates vitamin D is regulated!
  The main factors are:

• PTH (activates 1-alpha-hydroxylase)
• Negative feedback by high Serum calcium and phosphate concentrations (and vice versa)
• Fibroblast growth factor 23 (FGF23) (FGF23 inhibits renal production of 1,25-dihydroxyvitamin D)

#2020BSQ-NOV/Q09
When calcium is high, 1,25-dihydroxycholecalciferol synthesis is reduced and inactive 24,25-dihydroxycholecalciferol is produced instead.
Extrarenal synthesis of vitamin D occurs in granulomatous diseases such as sarcoidosis.

Main action is to 'mobilize calcium from bone' and increased renal phosphate excretion.

Unconjugated hyperbilirubinaemia can be cause by ileal resection because decreased resorption of bile salts allows them to enter the colon and solubilize the bilirubin (which has been unconjugated by gut bacteria)

Dubin Johnson syndrome

#autosomal-Recessive
Defect in active excretion of conjugated bilirubin from the liver.
Liver appears black!
Except for conjugated hyperbilirubinaemia, liver enzymes are normal!.
Patients are asymptomatic.
Rotor syndrome was initially considered to be a variant of this but it's a different disease.

Rotor syndrome

#autosomal-Recessive

[!INFO] Basis:
In Rotor syndrome, there is a defect in hepatic storage of conjugated bilirubin, which leaks into the plasma, resulting in hyperbilirubinemia.

• Rotor syndrome is an autosomal-recessive condition characterized by a predominantly conjugated hyperbilirubinemia.
• Patients are generally asymptomatic and jaundice may be an incidental finding.
• More than 50% of the serum bilirubin is conjugated and bilirubinuria is typically present.
• Symptomatically similar to Dubin-Johnson syndrome but the liver is histologically normal.
• A benign condition with a normal life expectancy, and no specific therapy is required.
• Source

#2020BSQ-NOV/Q07

#2020BSQ-NOV/Q01
Lactose is a disaccharide. Dietary intake decreases from infancy to adulthood.
It's broken down by intestinal lactase to glucose and galactose which are both absorbed by intestinal SGLT-1. Failure to break down lactose reads to passage into the colon where bacterial activity converts it to short chain fatty acids and hydrogen gas. -> symptoms of bloating, flatulence, diarrhoea few hours after ingesting lactose. Soluble end products of bacterial metabolism cause osmotic diarrhoea. Source
Secondary lactose intolerance can resolve after the initiating cause is removed.

Pathophysiology of cirrhocis

#2020BSQ-NOV/Q04

Mechanism of porto-systemic shunting

Some organs and tissues are drained by both portal veins and hepatic veins. Decreased flow through portal veins (due to portal hypertension) causes increased flow and congestion of the systemic veins.
Portal hypertension is defined as pressure > 5mmHg in the portal veins but becomes clinically significant after about 12 mmHg. Below 12, there is a significant reduction in risk of variceal bleeding.

Monro-kellie doctrine

#2020BSQ-NOV/Q11

[!INFO]
The answer to stem D in the question
Can't find a source explaining what happens to venous pressure when ICP is increased.
However, the following are interesting facts about cerebral venous drainage:

1. The dural sinuses don't have smooth muscle linings like the arteries.
2. They are easily collapsible when the ICP increases.
3. Collapse -> decreased venous flow -> back pressure -> oedema -> increased ICP -> vicious cycle.
4. The venous drainage of the brain does not have valves to the JVP is directly transmitted to the cerebral veins.
5. There is a negative pressure within the superior sagittal sinus (? and the other sinuses) in the sitting position so that air can be sucked in if they are opened during surgery.
6. A cervical collar can significantly increase the cerebral venous pressure.
   This article explains why venous outflow is a very important regulator of intra cranial pressure Source
   An article with a great diagram conceptualizing the Monro-kellie doctrine: Source

[!INFO] Elevated urobilinogen levels
#2020BSQ-NOV/Q04
Urobilinogen levels rise with increasing bilirubin production.
"Elevated urobilinogen levels may also be seen when the liver simply cannot remove urobilinogen from the portal venous blood, as occurs in severe liver disease, such as cirrhosis." - Source